We have previously demonstrated that the chemokine IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.
|Number of pages||9|
|Journal||Journal of Neuroimmunology|
|State||Published - 30 Apr 2009|
Bibliographical noteFunding Information:
This research was supported by grants from The Muscular Dystrophy Association of America (MDA), The Association Francaise Contre les Myopathies (AFM), The European Commission (LSHN-CT-2006-037833) and The Chief Scientist Office, Israel Ministry of Health.
- Experimental autoimmune myasthenia gravis (EAMG)
- IFN-γ inducible protein 10 (IP-10)
- Myasthenia gravis (MG)